Gene expression signatures in Tif1b, Hp1a or Hp1g knockdown hematopoietic progenitors
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE48897 | GEO | 2014/08/01
SECONDARY ACCESSION(S): PRJNA212232
REPOSITORIES: GEO
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Project description:Gene expression analyses of Tif1b, Hp1a or Hp1g knockdown hematopoietic progenitors. Growth of hematopoietic stem cells (HSCs) are significantly impaired upon knockdown of Hp1a and Hp1g. Results provide insight into the role of these factors in hematopoiesis. HSCs (CD34- c-Kit+ Sca1+ Lineage- ) were transduced with lentivirus expressing shRNA against Tif1b, Hp1a or Hp1g, and cultured for 14 days. Then, GFP+ c-Kit+ Lineage- hematopoietic progenitors were sorted and subjected into microarray analysis
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Project description:Gene expression signatures in Tif1b, Hp1a or Hp1g knockdown hematopoietic progenitors
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Project description:Heterochromatin protein 1a (HP1a) is a well-known component of pericentromeric and telomeric heterochromatin in Drosophila. However, its role and the mechanisms of its binding in the chromosome arms (ChAs) remain largely unclear. Here, we identified HP1a-interacting domains in the somatic cells of Drosophila ovaries using a DamIDseq approach and compared them with insertion sites of transposable elements (TEs) revealed by genome sequencing. Although HP1a domains cover only 13% of ChAs, they non-randomly associate with 42% of TE insertions. Furthermore, HP1a propagates from TE insertions at distances up to 10-kb. These data confirm the role of TEs in formation of HP1a islands in ChAs. However, only 18% of HP1a domains have adjacent TEs, indicating the existence of other mechanisms of HP1a domain formation besides spreading from TEs. In particular, many TE-independent HP1a domains correspond to the regions attached to the nuclear pore complexes (NPCs), or contain active gene promoters. Surprisingly, HP1a occupancy on the promoters of these genes does not lead to their repression. However, the steady-state transcript level of many genes located outside of HP1a domains was altered upon HP1a knockdown in the somatic cells of ovaries, thus pointing to the strong indirect effect of HP1a depletion. Collectively, our results support an existence of at least three different mechanisms of HP1a domain emergence in ChAs: spreading from TE insertions, interaction with the chromatin located near NPCs and targeting to the promoters of moderately expressed genes.
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Project description:Insertions of transposable elements (TEs) in eukaryotic genomes are usually associated with repressive chromatin, which spreads to neighbouring genomic sequences. In ovaries of Drosophila melanogaster, the Piwi-piRNA pathway plays a key role in the transcriptional silencing of TEs considered to be exerted mostly through the establishment of H3K9me3 histone marks recruiting Heterochromatin Protein 1a (HP1a). Here, using RNA-seq, we investigated the expression of TEs and the adjacent genomic regions upon Piwi and HP1a germline knockdowns sharing a similar genetic background. We found that the depletion of Piwi and HP1a led to the derepression of only partially overlapping TE sets. Several TEs were silenced predominantly by HP1a, whereas the upregulation of some other TEs was more pronounced upon Piwi knockdown and, surprisingly, was diminished upon a Piwi/HP1a double-knockdown. We revealed that HP1a loss influenced the expression of thousands of protein-coding genes mostly not adjacent to TE insertions and, in particular, downregulated a putative transcriptional factor required for TE activation. Nevertheless, our results indicate that Piwi and HP1a cooperatively exert repressive effects on the transcription of euchromatic loci flanking the insertions of some Piwi-regulated TEs. We suggest that this mechanism controls the silencing of a small set of TE-adjacent tissue-specific genes, preventing their inappropriate expression in ovaries.
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